Department of Molecular Biology and Genetics, Faculty of Arts and Sciences, Bingol University, Bingol, Turkey.
Neurochem Res. 2020 May;45(5):1064-1071. doi: 10.1007/s11064-020-02982-8. Epub 2020 Feb 10.
Accumulating evidences demonstrated that Reactive Oxygen Species (ROS) may lead to serious damages to numerous cellular biomolecules, consequently resulting in the development of several neurological diseases. Diclofenac (Dic), the most widely preferred non-steroidal anti-inflammatory drug (NSAID) induces apoptosis by an alteration in function of mitochondria and creation of ROS. Chrysin (Chr) is a naturally active component that is found in numerous plants and bee products and retains strong neuroprotective and antioxidant properties. However its effect of Dic induced injury on SH-SY5Y neuron cells have not been investigated to date. The goal of present research was to study the molecular mechanisms of Chr protection from oxidative injury caused by Dic in SH-SY5Y cells. Dic induced significant toxicity on the cells and this effect was reversed by pre-treatment with Chr. Dic triggered a noteworthy increase in the cellular ROS and Lipid peroxidation (LPO) levels and decrease in Total antioxidant status (TAS) level while pre-treatment with Chr reversed these effects. Dic induction increased the Bax, cytochrome c, cas-3, cas-8 and p53 expression at gene transcription level. Elevated levels of these genes considerably decreased by Chr pre-treatment revealing the defensive effects of Chr. The results obviously presented that exposure of SH-SY5Y with Dic resulted in oxidative stress and apoptosis while pre-treatment of neuron cells with Chr protects the cells against apoptosis triggered by Dic induction.
越来越多的证据表明，活性氧（ROS）可能对许多细胞生物分子造成严重损害，从而导致多种神经疾病的发生。双氯芬酸（Dic）是最广泛使用的非甾体抗炎药（NSAID），通过改变线粒体功能和产生 ROS 诱导细胞凋亡。白杨素（Chr）是一种天然存在于许多植物和蜂产品中的活性成分，具有很强的神经保护和抗氧化特性。然而，迄今为止，尚未研究 Chr 对 Dic 诱导的 SH-SY5Y 神经元细胞损伤的作用。本研究的目的是研究 Chr 对 Dic 诱导的 SH-SY5Y 细胞氧化损伤的保护作用的分子机制。 Dic 对细胞有显著的毒性作用，Chr 的预处理可逆转这种作用。 Dic 诱导细胞内 ROS 和脂质过氧化（LPO）水平显著增加，总抗氧化状态（TAS）水平降低，而 Chr 的预处理可逆转这些作用。 Dic 诱导可增加 Bax、细胞色素 c、cas-3、cas-8 和 p53 在基因转录水平的表达。Chr 预处理可显著降低这些基因的水平，揭示了 Chr 的保护作用。结果表明，Dic 暴露于 SH-SY5Y 可导致氧化应激和细胞凋亡，而 Chr 预处理可保护神经元细胞免受 Dic 诱导的细胞凋亡。
